PA5-23125

antibody from Invitrogen Antibodies

Targeting: TLR4 ARMD10, CD284, hToll, TLR-4

Western blot (Supportive data in Antibodypedia)

Immunohistochemistry (Recommended by provider)

Flow cytometry (Supportive data in Antibodypedia)

Other assay (Supportive data in Antibodypedia)

Antibody Data

Product number

PA5-23125

Provider

Invitrogen Antibodies

Product name

TLR4 Polyclonal Antibody

Antibody type

Polyclonal

Antigen

Synthetic peptide

Reactivity

Human, Mouse, Porcine

Host

Rabbit

Isotype

IgG

Vial size

100 µg

Concentration

1 mg/mL

Storage

-20° C, Avoid Freeze/Thaw Cycles

References

Submitted references

Electroacupuncture Improved Hippocampal Neurogenesis following Traumatic Brain Injury in Mice through Inhibition of TLR4 Signaling Pathway.

Ye Y, Yang Y, Chen C, Li Z, Jia Y, Su X, Wang C, He X
Stem cells international 2017;2017:5841814

Western blot

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Western blot analysis of TLR4 in partial recombinant mouse TLR4 protein. Samples were incubated in TLR4 polyclonal antibody (Product # PA5-23125) using a dilution of 2 µg/mL.

Flow cytometry

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Cell surface flow cytometric analysis using TLR4/CD284 polyclonal antibody (Product # PA5-23125). Mouse macrophage cells were probed using 1 µg of TLR4/CD284 polyclonal antibody (Product # PA5-23125) (red) and 1 µg of isotype control antibody (green). PE-conjugated secondary were used for this test.

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Flow cytometry of TLR4 in RAW cells. Samples were incubated in TLR4 polyclonal antibody (Product # PA5-23125) using a dilution of 2 µg. Antibody (conjugated to Alexa Fluor ® 488) (red) and 2 µg of isotype control antibody (green).

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Flow cytometry of TLR4 in Mouse macrophage cells. Samples were incubated in TLR4 polyclonal antibody (Product # PA5-23125) using a dilution of 1 µg followed by PE-conjugated secondary. Antibody (red) and 1 µg of isotype control antibody (green).

Other assay

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Figure 2 EA treatment inhibited the level of toll-like receptor 4 (TLR4) in the hippocampus after TBI. (a) Representative Western blot (WB) bands of hippocampal TLR4 expression in the sham, TBI, TBI + EA, and sham + EA groups ( n = 9 in each group) at 21, 28, and 35 days posttrauma. (b) Quantitative analysis suggested that hippocampal TLR4 protein significantly increased in the TBI group compared with the sham group. And EA treatment caused an evident suppression of TBI-induced TLR4 upregulation in the TBI + EA group compared with the TBI and sham + EA groups. * P < 0.05 versus the TBI group.

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Figure 5 EA treatment exerted an inhibitory effect on both of the two downstream pathways of TLR4 in the hippocampus posttrauma. Hippocampal TLR4, Myd88, TRAF6, TRAM, TRIF, and NF- kappa B expression of the sham, TBI, TBI + EA, TBI + EA + LPS, TBI + EA + Veh, and sham + EA groups ( n = 3 in each group) were detected by WB at 35 days after TBI. (a-f) The six kinds of proteins in TLR4/Myd88 kappa B and TLR4/TRIF/ kappa B signaling pathways were upregualted in the TBI group compared with the sham group and the sham + EA group. EA treatment resulted in a significant decrease in the TBI + EA group, but the effects were attenuated by LPS administration in the TBI + EA + LPS group. No difference of the proteins between the TBI + EA and TBI + EA + Veh groups was observed. * P < 0.05 versus the TBI group, + P < 0.05 versus the TBI + EA + LPS group.